1. We have isolated cellular mutants resistant to transformation by Kirsten and Harvey murine sarcoma viruses. NIH/313 cells containing 2 copies of Kirsten sarcoma virus and mutagenized with MNNG gave rise to flat revertant cells which contained both copies of the Kirsten virus genome, rescuable sarcoma virus, and high levels of the viral protein p21. The revertant phenotype was dominant in cellular hybrids formed after PEG fusion of flat revertants with Kirsten and Harvey virus-transformed cells. Fusion of the revertants with any of several cell lines transformed by other viruses, both RNA and DNA containing, and by chemically transformed cells resulted in the formation of hybrid cells with a transformed phenotype. The results indicate that the Kirsten sarcoma virus revertants isolated here are mutants in a cellular gene. 2. Cells transformed by a molecular chimera formed by the ligation of v-ras, a gene which codes for the p21 protein responsible for transformation by Kirsten and Harvey sarcoma viruses, and the Long Terminal Repeat of MMTV, which confers susceptibility to glucocorticoid hormone regulation on nearby genes, were adapted to growth in serum-free culture conditions in preparation for quantitative studies on hormone interactions with regulatory MMTV sequences.